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Clinical Consultation: Deep Tissue Injury
Deep tissue injury (DTI) is a term proposed by the National Pressure Ulcer Advisory Panel (NPUAP) to describe a unique type of pressure ulcer not captured under current staging guidelines. DTI ulcers have been described as purple pressure ulcers, ulcers likely to deteriorate, and bruises over bony prominences (Ankrom et al., 2005). Descriptions of DTI in the literature include those by Paget (1873), who reported purple areas with tissue sloughing and large cavities once open, and Black and Black (2003), who described a wound on the sacrum of a 67-year-old woman in the intensive care unit postoperatively. Groth (1942) reported creating deep “malignant pressure sores” in an animal model. Even Shea (1975), who is credited with describing pressure ulcers according to depth and whose system was later revised and adapted by the NPUAP, described ulcers that appear superficial but conceal a deeper lesion. However, he did not include these lesions in his staging system.
DTI commonly presents over bony prominences and may initially appear as bruises or deep purple lesions. Risk factors for DTI include prolonged pressure and impaired perfusion. NPUAP has proposed the following definition for DTI: “A pressure-related injury to subcutaneous tissues under intact skin. Initially these lesions have the appearance of a deep bruise. These lesions may herald the subsequent development of a Stage III–IV pressure ulcer even with optimal treatment” (NPUAP, 2002).
It is important to have a mechanism to classify DTI because the current staging system does not adequately describe the pathophysiology of these ulcers. When a patient presents with DTI, the epidermis is intact over the bony prominence, but there is an appearance of discolored tissue beneath the epidermis. Therefore, according to the current NPUAP staging system, this would classify as a Stage I ulcer.
Ulcers attributed to DTI rapidly deteriorate from the appearance of intact epidermis to deep Stage III–IV ulcers. It is postulated that this rapid deterioration is a combination of direct ischemic injury and reperfusion injury, although the precise pathogenesis is unknown (Black & Black, 2003).
Labeling DTI as a Stage I ulcer could misrepresent it as a minor lesion with resolution likely to occur with offloading. However, if the subcutaneous tissue damage has already occurred and additional damage potentially occurs during reperfusion, it is likely that no amount of pressure redistribution will prevent further deterioration of the wound. Labeling DTI as a Stage II ulcer on early presentation is also inadequate because the lesion will deteriorate. Likewise, labeling DTI as unstageable is ambiguous because intact purple lesions over bony prominences are not appropriate for debridement. There are multiple inherent problems with the current pressure ulcer staging system, including doubt about whether the current system actually reflects an ulcer’s clinical progression and lack of definitive evidence about the process of pressure ulcer evolution (the top-down theory vs. the bottom-up theory) (Doughty et al., 2006). The top-down theory postulates that pressure ulcer damage begins from the top (the epidermis) and progresses to deeper tissue levels. The bottom-up theory postulates that pressure ulcer damage begins at the bone and muscle interface (the bottom) and takes time for the damage to be recognized at the epidermal level. Might superficial ulcers caused by friction and moisture be top-down ulcers, and ulcers caused by pressure and shear resulting in greater depth of tissue destruction be bottom-up ulcers?
At the consensus conference held by the NPUAP in February 2007, a definition for suspected DTI was determined. Suspected DTI is “purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. Further description—DTI may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.” (NPUAP, Feb. 2007). Documentation should include a description of the wound’s presentation and ongoing description of the sequential deterioration of the wound. Chronological photographs, according to your institution’s policy and procedure, are helpful to demonstrate initial presentation and ongoing deterioration of the wound despite pressure dispersion interventions. Pressure dispersion interventions should include repositioning, avoiding positioning on the wound, and possibly alternative support surfaces (e.g., mattresses, cushions), depending on the anatomical location of the wound.
About the Author
Mary Arnold Long, MSN RN CRRN CWOCN APRN-BC CLNC, is a clinical nurse specialist at Drake Center in Cinncinnati, OH. Contact her at firstname.lastname@example.org
Ankrom, M. A., Bennett, R. G., Sprigle, S., Langemo, D., Black, J. M., Berlowitz, D. R., et al. (2005). National Pressure Ulcer Advisory Panel pressure-related deep tissue injury under intact skin and the current pressure ulcer staging system. Advances in Skin & Wound Care, 18(1), 35–42.
Black, J. M., & Black, S. B. (2003). Deep tissue injury. Wounds, 15(11), 380.
Doughty, D., Ramundo, J., Bonham, P., Beitz, J., Erwin-Toth, P., Anderson, R., et al. (2006). Issues and challenges in staging of pressure ulcers. Journal of Wound, Ostomy and Continence Nursing 33(2), 125–132.
Groth, K. E. (1942). Clinical observations and experimental studies of the pathogenesis of decubitus ulcers. Acta Chirurgica Scandinavica, 76(Suppl.), 1–209.
NPUAP. (2002). Deep Tissue Injury Task Force. Reston, VA: National Pressure Ulcer Advisory Panel NPUAP. Updated Staging System. Retrieved February, 2007 from www.npuag.org
Paget, J. (1873, May 10). Clinical lecture on bed-sores. Student Journal and Hospital Gazette, pp. 144–146.
Shea, J. D. (1975). Pressure sores. Clinical Orthopaedics and Related Research, 112, 89–100.